Age-related macular degeneration (AMD), a leading cause of blindness worldwide, is as prevalent as cancer in industrialized nations. Most blindness in AMD results from invasion of the retina by choroidal neovascularization (CNV). AMD affects 30-50 million people globally, with approximately 90% of severe vision loss attributed to CNV (Ambati, J., et al., Surv Ophthalmol. 48, 257-293 (2003)). The worldwide prevalence of CNV is expected to double in the next decade due to population aging. Targeting the pro-angiogenic cytokine vascular endothelial growth factor (VEGF)-A has been validated in patients with CNV (Gragoudas, et al. N Engl J. Med. 351, 2805-2816 (2004); Brown. et al. N Engl J. Med. 355, 1432-1444 (2006); Rosenfeld, et al. N Engl J. Med. 355, 1419-1431 (2006)). However, substantial improvement of vision occurs only in one-third of patients treated with VEGF-A antagonists, and one-sixth of treated patients still progress to legal blindness. Moreover, safety concerns with continual (Brown, et al. N Engl J. Med. 355, 1432-1444 (2006)) blockade of VEGF-A, which is constitutively expressed in the normal adult human retina Famiglietti et al. Brain Res. 969, 195-204 (2003)), are emerging Nishijima et al., Am J. Pathol. 171, 53-67 (2007); Saint-Geniez et al., PLoS ONE. 3, e3554 (2008)). Thus, treatment strategies based on more specific targeting of CNV are desirable. However, no molecular marker specific for human CNV has yet been reported.